Effect of Thyroxine on the Hepatic Glycogen and Glucose-6-Phosphatase Activity of Developing Rats

Paul, A. K.; Dhar, Anju

doi:10.1055/s-2007-996262

Cited by 9 publications

(4 citation statements)

References 5 publications

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“…Previous studies in the dog (40) and rat (42) have shown a decrease in both liver and muscle glycogen stores in response to excess thyroid hormones. In man, however, the evidence is more uncertain.…”

Section: Glucose Homeostasismentioning

confidence: 83%

The Effect of Thyroid Hormones on Gluconeogenesis and Forearm Metabolism in Man

Sandler

Robinson

Rabin

et al. 1983

The Journal of Clinical Endocrinology & Metabolism

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The present study was designed to examine the effects of excess T3 on total body glucose production and forearm exchange of glucose, amino acids, and other metabolites. Five healthy male volunteers were studied after an overnight fast, before and 7 days after the administration of 150 micrograms/day T3. Glucose production (milligrams per kg/min) was measured using a primed continuous infusion of [3-3H]glucose and gluconeogenic index (micromoles per kg/min) was measured by following the conversion of infused [14C]alanine to [14C]glucose. Blood flow across the forearm was measured using capacitance plethysmography and forearm release of substrates was determined by the Fick principle. After T3 administration, there was a 3.7-fold rise in T3 from 150 +/- 15 to 530 +/- 12 ng/dl (P less than 0.001), with no change in insulin (12 +/- 1 microU/ml pre-T3 vs. 13 +/- 2 microU/ml post-T3) and glucagon (79 +/- 5 pre-T3 vs. 84 +/- 7 pg/ml post-T3). T3 administration resulted in an increase in plasma glucose (from 83 +/- 5 to 98 +/- 5 mg/dl; P less than 0.05), net glucose uptake by the forearm (from 250 +/- 90 to 712 +/- 60 nmol/100 ml forearm tissue X min; P less than 0.005) and glucose production (1.7 +/- 0.09 to 2.2 +/- 0.08 mg/kg X min; P less than 0.005), without a change in glucose clearance (2.1 +/- 0.02 vs. 2.0 +/- 0.02 ml/kg X min); the rate of conversion of [14C]alanine to [14C]glucose increased by 30% (0.56 +/- 0.03 to 0.74 +/- 0.03 mumol/ kg X min P less than 0.005). These values were associated with a 25% increase in blood lactate to 712 +/- 69 mumol/liter (P less than 0.05) and a 131% increase in lactate release across the forearm to 434 +/- 90 (P less than 0.005). Forearm release of alanine (96 +/- 29 nmol/100 ml forearm tissue X min) and glutamine (151 +/- 41 nmol/100 ml forearm tissue X min) increased by 90% (P less than 0.005 and P = 0.04, respectively), with no change in their concentrations. Forearm release of branched chain amino acids did not change, while those of their ketoacids, alpha-ketoisocaproate (KIC) and alpha-ketoisovalerate (KIV), doubled (to 64 +/- 9 mumol/liter for KIC and 39 +/- 6 mumol/liter for KIV; P less than 0.05). These were associated with a 45% increase in the branched chain amino acid levels and a 46% rise in both KIC and KIV levels to 41 +/- 9 and 28 +/- 7 mumol/liter, respectively (P less than 0.05). There was a concurrent significant (P less than 0.05) change in the arterial levels of phenylalanine (-32%), tyrosine (-29%), threonine (-20%), glycine (-20%), and serine (-15%), without any change in their efflux across the forearm. The data indicate that a pharmacologically induced rise in T3, to levels comparable to those seen in hyperthyroidism, results in enhanced glucose production, with an increase in glucose uptake by the forearm. The former can be partially accounted for by an increase in hepatic gluconeogenesis, glycogenolysis, or possibly increased renal glucose production...

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Section: Glucose Homeostasismentioning

confidence: 83%

The Effect of Thyroid Hormones on Gluconeogenesis and Forearm Metabolism in Man

Sandler

Robinson

Rabin

et al. 1983

The Journal of Clinical Endocrinology & Metabolism

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“…Hypophysectomized rats treated for 4 days with 0.1 mg T 4 daily also have been shown to increase the glucose-6-phosphatase activity (Harper and Young 1959). The suppression of enzyme activity was found in rats treated with 0.1 mg T 4 for 5 days (Paul and Dhar 1980) as well as in mice receiving T 3 (0.03; 0.3,3 ugm daily) (Winnick 1970) by the intraperitoneal route for 6 days. Considering the animal species employed, nutritional status of animals, type and duration of treatment we have not been able to find a satisfactory explanation for these contradictory reports.…”

Section: Discussionmentioning

confidence: 95%

“…Earlier studies have demonstrated that the activities of the translocase and hydrolase components of glucose-6-phosphatase is augmented in fasted (Arion andNordlie 1965;Fisher and Stetten 1966;Nordlie, Arion, Hanson, Gildsdorf and Home 1968) and in diabetic animals (Jakobsson and Dallner 1968) and that glucocorticoids and glucagon increase the enzyme activity both in vivo (Arion and Nordlie 1967) and in vitro (Speth and Schulze 1981). The action of thyroid hormones on glucose-6-phosphatase has been previously studied in rats and mice and stimulatory as well as inhibitory effects have been reported (Murad andFreedland 1967,Paul andDhar 1980;Winnick 1970). In the present study we have investigated the effect of thyroxine (T 4 ) and triiodothyronine (T 3 ) on the activities of the translocase and hydrolase components of hepatic glucose-6-phosphatase in fed and fasted rats.…”

mentioning

confidence: 99%

Effect of Thyroid Hormones on the Activity of Hepatic Glucose-6-Phosphatase in Fed and Fasted Rats

Khan

Löw²,

Efendić³

1987

Horm Metab Res

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The action of thyroid hormones on hepatic glucose-6-phosphatase was studied in rats. Fed and 24-h fasted rats received T3 (10 micrograms/day) or T4 (25 micrograms/day) 1 h, 1 or 3 days before sacrificing. In addition a group of fed rats was treated with T4 for 7 and 14 days. The glucose-6-phosphatase activity was measured in the isolated microsomes prepared from the liver. The intactness of the microsomal preparation was checked using 2 mM mannose-6-phosphate as a substrate. In fed rats a single injection of T3 or T4 augmented the activities of the translocase and hydrolase components of glucose-6-phosphatase provided that the rats were killed 24 h after the administration of hormone. This effect was more pronounced in animals treated for 3-14 days. As expected, fasting per se increased the activities of both components of the enzyme. Moreover, in fasted rats treatment with T3 and T4 for 3 days further augmented the activities of the translocase and the hydrolase components of glucose-6-phosphatase. In fed animals T3 and T4 increased the latency of the enzyme whereas in fasted animals thyroid hormones increased the activities of the translocase and hydrolase components in parallel, maintaining the level of latency of the enzyme system. Administration of T3 and T4 increased blood glucose level in fasted rats after one day, while in fed rats a significant hyperglycaemia appeared after 7-14 days of treatment. In conclusion, T3 and T4 increase the activities of the translocase and hydrolase components of hepatic glucose-6-phosphatase in fed and fasted rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…6 Hyperthyroidism may aggravate the basic metabolic disturbance in AIP by further increasing hepatic 5-aminolaevulinate (ALA) synthase activity, as physiological levels of thyroid hormones stimulate allylisopropylacetamide-induced porphyrin biosynthesis in chick embryo liver cell culture. 7 Furthermore, hyperthyroidism is a catabolic disease causing an increase in energy demand and depletion in glycogen stores, 8 and starvation is known to precipitate symptomatic AIP. In our patient, both attacks occurred in the luteal phase of the menstrual cycle and recurrent attacks in the late luteal phase can be a major problem.…”

Section: Discussionmentioning

confidence: 99%